Evidence map›Paper›PMID 39436921›Full record

ArticleThe oncologist2025

Clinical impact of TP53 functional mutations in patients with metastatic colorectal cancer treated with bevacizumab and chemotherapy.

Annamaria Ruzzo, Francesco Graziano, Silvia Palladino, Nicholas W Fischer, Vincenzo Catalano, Paolo Giordani, David Malkin, Tiziana Tamburrano, Alberto Patriti, Filippo Petrelli and 2 more

Abstract read
In one paragraph

Article in The oncologist, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Annamaria RuzzoDepartment of Biomolecular Sciences, University of Urbino, 61029 Urbino, Italy.ORCID 0000-0003-2815-1890
Francesco GrazianoMedical Oncology Unit, AST1, 61121 Pesaro, Italy.
Silvia PalladinoDepartment of Biomolecular Sciences, University of Urbino, 61029 Urbino, Italy.ORCID 0009-0001-3498-6555
Nicholas W FischerGenetics & Genome Biology Program, The Hospital for Sick Children, Toronto, M5G 0A4, Canada.
Vincenzo CatalanoMedical Oncology Unit, AST1, 61029 Urbino, Italy.
Paolo GiordaniMedical Oncology Unit, AST1, 61121 Pesaro, Italy.
David MalkinGenetics & Genome Biology Program, The Hospital for Sick Children, Toronto, M5G 0A4, Canada.
Tiziana TamburranoMedical Oncology Unit, AST1, 61121 Fano, Italy.
Alberto PatritiGeneral Surgery Unit, AST1, 61121 Pesaro, Italy.
Filippo PetrelliGeneral Surgery Unit, AST1, 61121 Pesaro, Italy.
Donatella SartiMedical Oncology Unit, AST1, 61029 Urbino, Italy.
Rita ChiariMedical Oncology Unit, AST1, 61121 Pesaro, Italy.

Funding

FanoAteneo Association (Fano, Italy)
6 · The paper itself

Abstract

backgroundClinical and experimental studies indicate that the tumor protein p53 (TP53) gene loss of function due to missense mutations (MMs) may confer sensitivity to anti-angiogenics. This effect seems to be linked to cross-talk mechanisms among TP53, vascular endothelial growth factor (VEGF), and VEGF receptors. We investigated whether specific TP53 MMs are associated with clinical outcomes of patients with metastatic colorectal cancer (mCRC) treated with first-line chemotherapy plus Bevacizumab. The study focused on KRAS-mutated, liver-only mCRC cases as a homogeneous subgroup that may represent a relevant setting for exploring this association. MATERIALS AND

methodsMMs were identified on primary tumors. MMs were classified by mutant-specific residual transcriptional activity scores (TP53RTAS) as transcriptionally inactive (TP53inactive = TP53RTAS 0%) or active (TP53active = TP53RTAS ≥ 1%) and used for stratifying patients in progression-free survival (PFS), response rate, and overall survival (OS) analyses.

resultsThe study population consisted of 62 patients. MMs were found in 39 cases (62%) with 16 having TP53inactive and 23 TP53active MMs. Patients with TP53inactive MMs showed better PFS in comparison with the remaining groups (wild-type and TP53active). This effect was retained in the multivariate model. A similar clinical impact was observed in the OS analysis. There was a significant difference in the overall response rate and rate of post-treatment resection of liver metastases between the TP53inactive and the wild-type or TP53active MMs cases.

conclusionsSpecific TP53 MMs may identify sub-groups of patients who benefit from Bevacizumab-based systemic therapy and these findings could lead to novel tailored treatment strategies in this setting.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsBevacizumabColorectal NeoplasmsTumor Suppressor Protein p53AdultAgedAged, 80 and overFemaleHumansLiver NeoplasmsMaleMiddle AgedMutationNeoplasm MetastasisBevacizumabTP53 protein, humanTumor Suppressor Protein p53Bevacizumabcolorectal cancerliver metastasismissense mutationTP53

Identifiers

PMID39436921
PMCPMC11954512

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.